To examine the physiological deficit to adrenergic stimulation with aging, 5 younger adult (3q1 year old) and 9 older adult (17q1 year old) healthy monkeys were studied after instrumentation with a left ventricular (LV) pressure gauge, aortic and left atrial catheters, and aortic flow probes to measure cardiac output directly. There were no significant changes in baseline hemodynamics in conscious older monkeys. For example, isovolumic contraction, LV dP/dt, was similar (3191q240, young vs. 3225q71 mmHg/sec), old as well as isovolumic relaxation, tau, (24.3q1.7msec, young vs. 23.0q1.0 msec, old). However, inotropic, lusitropic and chronotropic responses to isoproterenol (ISO)(0.1 fg/kg), norepinephrine (NE)(0.4 fg/kg), and forskolin (FOR)(75 nmol/kg) were significantly (p<0.05) depressed in older monkeys. For example, ISO increased LV dP/dt by by 146q14% in younger monkeys and by only 70q5% in older monkeys. ISO also reduced tau more in younger monkeys (-28q7%) as compared with older monkeys (-13q3%). Furthermore, peripheral vascular responsiveness to ISO, NE, FOR, and phenylephrine (PE)(5 fg/kg) was significantly (p<0.05) reduced in older monkeys. For example, phenylephrine, 5 fg/kg, increased total peripheral resistence by 69q4% in younger monkeys and by only 45q3% in older monkeys. Thus, in older monkeys without associated cardiovascular disease, baseline hemodynamics are preserved, but adrenergic receptor responsiveness is reduced systemically, not just in the heart.